Evidence map›Paper›PMID 34681949›Full record

ReviewInternational journal of molecular sciences2021

EHMT2/G9a as an Epigenetic Target in Pediatric and Adult Brain Tumors.

Barbara Kunzler Souza, Natalia Hogetop Freire, Mariane Jaeger, Caroline Brunetto de Farias, Algemir L Brunetto, André T Brunetto, Rafael Roesler

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.3field-weighted citation impact, top 20% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Histone Methyltransferases G9a/International journal of molecular sciences · 2023
    Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. An interplay between BRD4 and G9a regulates skeletal myogenesis.Frontiers in cell and developmental biology · 2022
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Barbara Kunzler SouzaCancer and Neurobiology Laboratory, Experimental Research Center, Clinical Hospital (CPE-HCPA), Federal University of Rio Grande do Sul, Porto Alegre 90035-003, Brazil.
Natalia Hogetop FreireCancer and Neurobiology Laboratory, Experimental Research Center, Clinical Hospital (CPE-HCPA), Federal University of Rio Grande do Sul, Porto Alegre 90035-003, Brazil.
Mariane JaegerCancer and Neurobiology Laboratory, Experimental Research Center, Clinical Hospital (CPE-HCPA), Federal University of Rio Grande do Sul, Porto Alegre 90035-003, Brazil.
Caroline Brunetto de FariasCancer and Neurobiology Laboratory, Experimental Research Center, Clinical Hospital (CPE-HCPA), Federal University of Rio Grande do Sul, Porto Alegre 90035-003, Brazil.
Algemir L BrunettoCancer and Neurobiology Laboratory, Experimental Research Center, Clinical Hospital (CPE-HCPA), Federal University of Rio Grande do Sul, Porto Alegre 90035-003, Brazil.
André T BrunettoCancer and Neurobiology Laboratory, Experimental Research Center, Clinical Hospital (CPE-HCPA), Federal University of Rio Grande do Sul, Porto Alegre 90035-003, Brazil.
Rafael RoeslerCancer and Neurobiology Laboratory, Experimental Research Center, Clinical Hospital (CPE-HCPA), Federal University of Rio Grande do Sul, Porto Alegre 90035-003, Brazil.ORCID 0000-0001-6016-2261
Universidade Federal do Rio Grande do Sul · BR

Funding

Children's Cancer Institute Not ApplicableEpigenica Biosciences Not ApplicableNational Council for Scientific and Technological Development (CNPq, MCTI, Brazil) 305647/2019-9National Council for Scientific and Technological Development (CNPq, MCTI, Brazil) 407765/2017-4Rio Grande do Sul State Research Foundation (FAPERGS, RS, Brazil) 17/2551-0001 071-0
6 · The paper itself

Abstract

Epigenetic mechanisms, including post-translational modifications of DNA and histones that influence chromatin structure, regulate gene expression during normal development and are also involved in carcinogenesis and cancer progression. The histone methyltransferase G9a (euchromatic histone lysine methyltransferase 2, EHMT2), which mostly mediates mono- and dimethylation by histone H3 lysine 9 (H3K9), influences gene expression involved in embryonic development and tissue differentiation. Overexpression of G9a has been observed in several cancer types, and different classes of G9a inhibitors have been developed as potential anticancer agents. Here, we review the emerging evidence suggesting the involvement of changes in G9a activity in brain tumors, namely glioblastoma (GBM), the main type of primary malignant brain cancer in adults, and medulloblastoma (MB), the most common type of malignant brain cancer in children. We also discuss the role of G9a in neuroblastoma (NB) and the drug development of G9a inhibitors.

Indexed as

DNA MethylationEpigenesis, GeneticAntineoplastic AgentsBrain NeoplasmsGene Expression Regulation, NeoplasticHistocompatibility AntigensHistone-Lysine N-MethyltransferaseHumansAntineoplastic AgentsEHMT2 protein, humanHistocompatibility AntigensHistone-Lysine N-Methyltransferasebrain tumorEHMT2epigeneticsG9aglioblastomamedulloblastoma

Identifiers

PMID34681949
PMCPMC8539543
OpenAlexW3206748858

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.